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ORIGINAL ARTICLE
Neuromuscular complications after hematopoietic stem
cell transplantation
Susanne Koeppen & Abhiyrahmi Thirugnanasambanthan &
Michael Koldehoff
Received: 19 December 2013 /Accepted: 20 March 2014 /Published online: 29 March 2014
# Springer-Verlag Berlin Heidelberg 2014
Abstract
Purpose The aim of this study was to analyze the occurrence
of neuromuscular symptoms in recipients of allogeneic hema-
topoietic stem cell transplantation (HSCT) for treatment of
malignant hematopoietic disease.
Methods Among 247 outpatients after allogeneic HSCT, we
conducted a prospective non-interventional study between
July 2011 and August 2013. During follow-up visits, clinical
and electrophysiological findings were correlated to the pres-
ence of autoantibodies/alloantibodies and to frequencies of
lymphocyte subpopulations in peripheral blood.
Results Resulting in an incidence of 8.1 %, 20 patients were
diagnosed with neuromuscular complications at a median
onset of 12 months post-transplant. Five patients (25 %) were
identified with polyneuropathy (PNP), ten patients (50 %)
with combined PNP and myopathy, four patients (20 %) with
myopathy or polymyositis (PM), and one patient (5 %) with
myasthenia gravis (MG). Immune-mediated sensorimotor
PNP after HSCT is characterized by a predominantly axonal
lesion and can be overlapping with neurotoxic side effects.
The latency between HSCT and development of PM varied
between 60 days and 72 months. In general, PM occurs
parallel to graft-versus-host disease (GvHD) after tapering of
immunosuppressive medication. Typical clinical features are
proximal bilateral limb weakness with muscle atrophy. Auto-
antibodies (Ab) were detected in 12 patients, myositis-specific
Ab only in one patient. In patients with progressive
neurological symptoms, a decrease in the CD4/CD8 T cell
ratio was observed.
Conclusions GvHD-related myositis appeared similar to idi-
opathic myositis regarding clinical and electromyographical
findings. As outcome measure, sequential analysis of lympho-
cyte subpopulations in peripheral blood seems to be more
suitable than Ab measurements. Whereas peripheral neuropa-
thies are commonly observed shortly after HSCT, MG is a rare
complication in the late post-HSCT phase.
Keywords Allogeneic hematopoietic stem cell
transplantation . Graft-versus-host disease . Polyneuropathy .
Polymyositis . Myasthenia gravis
Abbreviations
AChR Ab Acetylcholine receptor antibody
AL Acute leukemia
ALL Acute lymphocytic leukemia
ANA Antinuclear antibodies
AML Acute myeloid leukemia
Ab Autoantibodies
CK-MB Creatine kinase-MB
CLL Chronic lymphocytic leukemia
CML Chronic myeloid leukemia
GvHD Graft-versus-host disease
HSCT Hematopoietic stem cell transplantation
ND Not done
MCL Mantle cell lymphoma
MG Myasthenia gravis
MM Multiple myeloma
MPN Myeloproliferative neoplasm
OMF Osteomyelofibrosis
PM Polymyositis
PNP Polyneuropathy
S. Koeppen (*): A. Thirugnanasambanthan
Department of Neurology, Medical School, University of
Duisburg-Essen, Hufelandstraße 55, 45122 Essen, Germany
e-mail: susanne.koeppen@uni-essen.de
M. Koldehoff
Department of Bone Marrow Transplantation, West German Cancer
Center, Medical School, University of Duisburg-Essen, Essen,
Germany
Support Care Cancer (2014) 22:2337–2341
DOI 10.1007/s00520-014-2225-0
Introduction
Allogeneic hematopoietic stem cell transplantation (HSCT)
has been shown to provide long-term disease-free survival for
otherwise fatal malignant or non-malignant hematological
disorders. With increasing survival rates due to toxicity-
reduced HSCT methods and advanced graft-versus-host dis-
ease (GvHD) management as well as improved antiinfectious
therapy and prophylaxis, a distinct increment in late
transplant-related complications can be observed. Early or
delayed neurological complications usually associated with
GvHD occur in 30–60 % of allogeneic HSCT recipients
[1–3]. Acute GvHD and chronic GvHD remain the major
causes of non-relapse mortality, and T cell alloreactivity has
been established as the primary cause of GvHD. The extent of
these complications can vary depending on the type of hema-
tologic disease, stage of diagnosis, age of the transplant pa-
tient, and whether the donor is major histocompatibility com-
plex (MHC) matched or mismatched to the recipient [4, 5].
According to the National Institutes of Health (NIH) consen-
sus criteria, neurological complications associated with
GvHD affect the central or peripheral nervous system or the
musculoskeletal system [6–10]. The most commonly recog-
nized GvHD-related neuromuscular manifestations include
polyneuropathy (PNP), less frequently myopathy, and myas-
thenia gravis (MG) [11–14]. Autoimmune/alloimmune mech-
anisms play a major role in the pathogenesis of neuromuscular
symptoms in the context of GvHD. However, metabolic and
drug-related factors may contribute to the neurologic impair-
ment. The aim of this study was to investigate the incidence
and clinical course of neuromuscular symptoms following
allogeneic HSCT. We also investigated the relationship be-
tween clinical features and laboratory findings.
Methods
Among patients with malignant hematologic disease who
underwent allogeneic HSCT at the West German Cancer
Center, University of Essen, Germany, between July 2011
and March 2013, 20 patients with GvHD-associated neuro-
muscular symptoms were included in this prospective non-
interventional study and followed until August 2013. The
source population in this period included 429 allogeneic
transplant patients, median age 54, and range 17–74 years.
A total of 182 patients with active infectious diseases or
malignancy relapse or who could not tolerate electrophysio-
logical evaluation (n=2) were excluded. The IRB of the
University of Essen approved the study, and written informed
consent was obtained from each patient. Medical records were
reviewed to determine diagnosis and treatment of the under-
lying hematologic disease, any comorbidity, the patient’s con-
dition prior to HSCT, and the clinical course until first
neurological evaluation. The neurological status was assessed
using the total neuropathy score (TNS), the Medical Research
Council (MRC) scale, hand grip strength measurements, fine
motor activity, coordinative function, and balance tests. To
assess symptoms of chemotherapy-induced peripheral neu-
ropathy, the quality of life questionnaire of the European
Organization for Research and Treatment of Cancer
(EORTC) was used (QLQ-CIPN20). Patients were available
for a neurological follow-up examination after a period of
approximately 3 months. In parallel, blood samples were
collected for serum creatine kinase (CK) measurement and
immunological investigations including testing for autoanti-
bodies (Ab) (ANA profile, ANCA-IFT, myositis profile,
AChR Ab) and determination of lymphocyte subpopulations
by flow cytometry. The antinuclear antibodies (ANA) were
detected by immunofluorescence and by immunoblotting.
Statistical analysis
For individual values, we selected the median and the range.
Continuous data are given as the mean with the standard
deviation (SD). Variations in data between the different groups
were tested either by a two-tailed unpaired t test or a Mann-
Whitney U test using the SPSS 11.5 program (SPSS Inc.,
Chicago, IL, USA).
Results
Twenty patients presented with neuromuscular complications
after allogeneic HSCT resulting in an incidence of 8.1 %.
Patient characteristics and laboratory findings are summarized
in the Table 1. The mean age of the patients was 50 years (49.9
±9.6 years, range 27–64). The median interval between first
evaluation and follow-up examination was 3 months. Due to
GvHD, all patients received immunosuppressive treatment
consisting of a calcineurin inhibitor and low-dose steroid
medication. The median time from transplant to the onset of
neuropathic symptoms was 12 months (range 2–120). The
latency between HSCT and development of PM varied be-
tween 60 days and 72 months. The most commonly reported
motor symptoms were weakness in 65 % and muscle cramps
in 55 % of the patients. The most frequent sensory symptoms
were paresthesia (60 %) and numbness (45 %). The major
clinical sign on neurologic examination was an impaired
vibration sense detected in 70 % of the patients. The mean
TNS score (range 0–36) was 8.97±4.5, the mean MRC sum
score (range 0–60) was 54.3±7.9, and the mean value of the
hand grip strength was 16.98±6.9 kp at baseline. Five patients
(25 %) were identified with PNP, ten patients (50 %) with
combined PNP and myopathy, four patients (20 %) with
myopathy or PM, and one patient (5 %) with MG.
2338 Support Care Cancer (2014) 22:2337–2341
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Support Care Cancer (2014) 22:2337–2341 2339
Electrophysiological testing including nerve conduction stud-
ies and electromyography, if possible, revealed an axonal
motor neuropathy of the peroneal nerve in 12 patients and a
sural nerve axonopathy in 6 patients. The maximum CK
serum concentration observed was 475 U/l. Ab were detected
in 12 patients, myositis-specific Ab only in one patient. Nine-
teen patients had hematopoietic full chimerism, and one pa-
tient had mixed chimerism. At the time of onset of neuromus-
cular symptoms, a coincidence with a decrease of CD4 T cells
and increase of CD8 T cells was observed in 17 and 12
patients, respectively.
Discussion
Improved survival of patients undergoing allogeneic HSCT
shifts the focus of neurologic involvement towards long-term
sequelae. Because of different new conditioning protocols of
allogeneic HSCT and immunosuppression, the nature of neu-
rologic complications has changed over time. In this study,
post-HSCT PNP in combination with myopathy appeared to
be more common than isolated myopathy or peripheral neu-
ropathy. Prior to the onset of PM, the immunosuppressive
medication had been tapered in all patients. PM following
HSCT has been reported to occur in approximately 3.4–
7.7 % of patients usually along with other manifestations of
GvHD [15]. In general, the onset is insidious, although it can
be acute especially after donor lymphocyte infusion (DLI)
[16]. Typical clinical features of PM are proximal bilateral
limb weakness and muscle atrophy, similar to idiopathic PM
[17]. The presence of Ab may correlate with the severity of
chronic GvHD [18]. In most cases, GvHD-related PM shows
a prompt treatment response to corticosteroids and cyclospor-
ine resulting in complete and sustained remission [19]. Nor-
mal or slightly elevated serum CK-levels in our patients are
compatible with clinical stability described in most cases.
Myositis-specific Ab were found in only one patient. This is
corresponding to previous reports [20]. MG has been de-
scribed as rare manifestation of chronic GvHD in the late
post-HSCT phase [21, 22]. However, circulating Ab directed
against muscle acetylcholine receptor (AChR Ab) are detect-
able in about 20 % of patients with chronic GvHD [23]. In our
patient with MG following HSCT, the onset of clinically overt
MG was associated with elevated AChR Ab and titin Ab. It is
noteworthy that titin Ab in the context of post-HSCT MG
have not been reported before. A considerable number of
patients in the present study complained of neuropathic symp-
toms correlated with other GvHD manifestations. However,
the pathogenesis of peripheral neuropathies following alloge-
neic HSCT is often multifactorial [24, 25]. Compared to prior
studies, the onset of PNP after HSCT showed a higher vari-
ability in our patients. Electrophysiological studies revealed a
predominantly axonal lesion of the peripheral nervous system
and chronic neurogenic or myogenic changes of the affected
muscles. None of our patients met the diagnostic criteria for
chronic inflammatory demyelinating polyneuropathy (CIDP).
The majority of patients were in stable clinical condition
during the observation period. Accordingly, laboratory testing
gave only little evidence of disease activity. Immunosuppres-
sive treatment was continued. However, our study has some
limitations. First, patients were not neurologically evaluated
prior to HSCT. Therefore, chemotherapy-induced PNP under-
lying a later developing GvHD-related affection of the periph-
eral nervous system cannot be excluded despite negative
history of neuropathic symptoms prior to HSCT. Second,
steroid myopathy might be a contributing factor of the motor
deficit in some patients because corticosteroids are the first-
line therapy of GvHD. In a retrospective analysis of patients
with acute myeloid leukemia or myelodysplastic syndrome
treated with high-dose steroid for acute GvHD following
allogeneic HSCT, steroid myopathy was identified in 41 %
of the patients [26]. Third, the small number of patients and
lack of a control group requires confirmation of the results in a
larger controlled prospective study. Despite these limitations,
it can be concluded from the results of this study based on the
partly longitudinal character of neurological evaluation that
the neuromuscular system seems to be affected more frequent-
ly than reported so far in patients with GvHD after allogeneic
HSCT. The immunological findings suggest that sequential
analyses of lymphocyte subpopulations in peripheral blood
might be helpful during the immunosuppressive dose reduc-
tion period in order to prevent GvHD-related clinical deterio-
ration. However, only further research studies can determine
whether it is possible to prevent those complications by
adapting the immunosuppressive regimen based on the lym-
phocyte subpopulation findings in the peripheral blood.
Conflict of interest The authors declare no conflict of interest. They
also state that they have full control of primary data and that they agree to
allow the journal to review their data if requested.
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- Neuromuscular complications after hematopoietic stem cell transplantation
Abstract
Abstract
Abstract
Abstract
Abstract
Introduction
Methods
Statistical analysis
Results
Discussion
References